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Biomedical subjects

S Suter

Publications and source records attributed to S Suter.

At least 91 records · Page 5Linked to original sources
PubMed1987

Dieldrin inhibition of gap junctional intercellular communication in rat glial cells as measured by the fluorescence photobleaching and scrape loading/dye transfer assays.

Application of the fluorescence-recovery after photobleaching (FRAP analysis) technique and scrape loading/dye transfer assay was made to measure the presence of gap junctional communication in primary rat glial cells in vitro in the presence and absence of the neurotoxicant and tumor promoter dieldrin, a chlorinated insecticide. Results demonstrate that primary rat glial cells are able to exhibit gap junctional intercellular communication and that dieldrin at noncytotoxic concentrations can modulate gap junctional communication as early as 10 min after exposure to the chemical and that the effect is reversible after 4 hr recovery from the dieldrin exposure. Both the FRAP analysis and the scrape loading/dye transfer assay have validated the observation that dieldrin inhibits gap junctional communication in other cell types using different techniques to measure gap junction function. These results were interpreted as an indication that inhibition of gap junctional communication might contribute to the cellular mechanism of dieldrin's neurotoxicity.

Animals↗
PubMed1987

Efficacy of inhaled amikacin as adjunct to intravenous combination therapy (ceftazidime and amikacin) in cystic fibrosis.

Eighty-seven patients with cystic fibrosis were admitted to hospital with an acute exacerbation of pulmonary symptoms associated with isolation of Pseudomonas aeruginosa from sputum. The patients were randomly allocated to receive intravenously administered ceftazidime (250 mg/kg/day) and amikacin (33 mg/kg/day) alone or with inhaled amikacin (100 mg twice a day). Other aspects of the 2-week treatment were constant. The two therapy groups were comparable in all aspects. At the completion of therapy, the addition of aerosolized amikacin produced temporary eradication of P. aeruginosa in 70% of the patients, compared with 41% in the intravenous therapy only group (P less than 0.02). Suppression of P. aeruginosa in sputum cultures was correlated with the amikacin sputum concentrations. However, both regimens resulted in similar improvements in clinical, radiologic, laboratory, and pulmonary function measurements, and within 4 to 6 weeks most patients were recolonized with P. aeruginosa. There was no serious toxicity or adverse effect. In patients with cystic fibrosis, the addition of aerosol aminoglycoside to systemic antipseudomonal combination therapy is not clinically beneficial.

Acute Disease↗
PubMed1986

Levels of free granulocyte elastase in bronchial secretions from patients with cystic fibrosis: effect of antimicrobial treatment against Pseudomonas aeruginosa.

Large amounts of free granulocyte elastase (GE), an enzyme capable of mediating airway damage, have been found in bronchial secretions of patients with cystic fibrosis who are infected with Pseudomonas aeruginosa. This finding indicates an imbalance between GE and its antiproteases, alpha 1-proteinase inhibitor (alpha 1-PI) and bronchial mucosal inhibitor (BMI), in the airways of these individuals. The effect of intravenous antimicrobial treatment against P. aeruginosa on activity and concentration of GE, BMI, and alpha 1-PI was evaluated in 30 treatment courses of 20 patients with cystic fibrosis. Although sputum volume and level of immunoreactive GE decreased and concentrations of alpha 1-PI and BMI increased significantly (P less than .05), a high level of free GE persisted. No active alpha 1-PI and BMI were detectable after treatment. High levels of GE correlated with a poor pulmonary condition (rs = .98, P less than .001). In vitro, elastolytic activity of bronchial secretions from patients with cystic fibrosis was significantly inhibited by eglin C and an oxidation-resistant variant of alpha 1-PI, both compounds currently produced by recombinant DNA technology.

Anti-Bacterial Agents↗
PubMed1986

Effect of the synthetic inhibitor tosylamino-phenylethyl-chloromethylketone on chemotactic peptide receptor activation and superoxide production in human neutrophils.

It was previously shown that inhibitors such as tosylamido-phenylethyl-chloromethylketone (TPCK) inhibit superoxide production by human neutrophils. These studies suggested that a chymotrypsin-like protease inhibited by TPCK was involved in the activation of the neutrophils oxidative system. In this study, we attempted to define the step in cellular activation and/or cell function inhibited by TPCK. TPCK 10(-5) M did not inhibit the following early events thought to be involved in the activation of oxidase. 1) f-met-leu-phe-induced activation of phospholipase C assessed by the production of inositol-tris-phosphate (IP3), 2) f-met-leu-phe-induced membrane potential changes, 3) f-met-leu-phe-induced increase in free cytosolic calcium, and 4) phorbol-myristate acetate-induced protein phosphorylation in 32P labeled neutrophils. We also showed that TPCK 10(-5) M inhibited bactericidal activity of neutrophils on Staphylococcus aureus, whereas it did not inhibit the ingestion rate of endotoxin-coated Oil red O particles. We conclude that 1) TPCK at the concentration of 10(-5) M inhibits superoxide production but not ingestion of Oil red O particles and 2) TPCK inhibits superoxide production at a step distal from calcium mobilization and protein phosphorylation. Radiolabeled TPCK may therefore be a useful tool to study, whether a protease is involved in the activation of the oxidative system distal to second messenger generation.

Adult↗
PubMed1986

Diagnostic and pathogenetic aspects of subacute sclerosing panencephalitis.

Subacute sclerosing panencephalitis, usually a rapidly progressive and fatal disease, is a slow virus infection, where measles virus persists in cells of the CNS and in lymphocytes. Four patients, 3 boys and 1 girl, are described, who presented a characteristic disease course, beginning at the age of 12 to 14 years after they had contracted measles infection during infancy or early childhood. The diagnostic criteria including clinical and laboratory CSF findings are summarized, and epidemiologic features related to measles and measles immunization are briefly discussed. In two patients specific measles virus protein antibodies in serum and CSF were analyzed. The results confirm postulated mechanisms for viral persistence in the CNS and suggest in addition a possible role of the viral protein H in the pathogenesis of SSPE.

Adolescent↗
PubMed1985

Intracellular calcium handling in cystic fibrosis: normal cytosolic calcium and intracellular calcium stores in neutrophils.

We used quin2, a high affinity fluorescent calcium indicator to measure free cytosolic Ca++ in neutrophils isolated from fresh heparinized blood of 13 cystic fibrosis (CF) patients (age range 6-32 yr) and 11 healthy individuals (age range 25-41 yr) as controls. The mean value of free cytosolic Ca++ for CF patients was 137 +/- 19 nM (mean +/- SD) and 141 +/- 23 nM for controls (p = NS). Calcium stores released after exposure of the cells to ionomycin in Ca++-free medium were also similar in neutrophils of CF patients (51 +/- 34 pmol/10(6) neutrophils) and in the controls (50 +/- 15 pmol/10(6) neutrophils). Stimulation of the neutrophils with the chemotactic peptide f-mlp (10(-7) M) led to similar rises in free cytosolic Ca++ with mean peak levels of 718 +/- 230 nM in CF patients and 687 +/- 321 nM in another population of 10 healthy adults. In our group of CF patients free cytosolic Ca++, intracellular Ca++ stores, and the kinetics of intracellular Ca++ transients induced by f-mlp are similar to those of normals. These findings do not support the hypothesis of a generalized defect in calcium handling at the cellular level in CF.

Adolescent↗
PubMed1984

Granulocyte neutral proteases and Pseudomonas elastase as possible causes of airway damage in patients with cystic fibrosis.

We studied the possible role of granulocyte neutral proteases as mediators of airway destruction in patients with cystic fibrosis (CF) who were infected with Pseudomonas aeruginosa. We measured the enzymatic activities of bronchial secretions on purified radioactively labeled complement component three (C3), elastin, and a granulocyte elastase-specific substrate. Bronchial secretions from 18 patients with CF who were infected with P aeruginosa had a significantly higher mean value for C3 cleaving, elastolytic, and granulocyte elastase-like activity than did two control groups. High enzymatic activities were observed in patients with CF who have advanced bronchial disease (that had been determined by a clinical scoring system). Kinetics of proteolysis of radioactively labeled C3 and inhibition profiles of the activities of the three enzymatic activities studied suggest that they are mainly derived from granulocytes. In addition, 20 of 31 strains of P aeruginosa isolated from patients with CF inactivated purified alpha 1-antiprotease in vitro. We postulate that granulocyte neutral proteases and P aeruginosa may act synergistically in the airways of patients with CF and may contribute to the destruction of elastin and inactivation of C3.

Adolescent↗
PubMed1984

Low levels of functional of alpha 1-proteinase inhibitor in the promotion of C3-cleavage by granulocyte-neutral proteases in pleural empyema.

It has been suggested that C3 breakdown by granulocyte-neutral proteases in pleural empyemas may be related to a decreased inhibitor potential for these enzymes. In the present study it was shown that in 17 infected pleural effusions, high proteolytic activity on 125I-labeled C3 (16.3% +/- 4.4%) correlated with low functional levels of alpha 1-proteinase inhibitor (alpha 1-PI), as determined by trypsin-inhibitory capacity (56.2 +/- 20.1 IU/ml; rs = -0.97, P less than .001), whereas in 18 sterile pleural effusions there was no such correlation (125I-labeled C3 cleavage, 2.2% +/- .2%; trypsin-inhibitory capacity, 192.6 +/- 26.7 IU/ml). However, alpha 1-PI and alpha 2-macroglobulin protein concentrations in infected and sterile effusions (as measured by immunodiffusion) were similar. Fifteen strains of three bacterial species--Streptococcus pneumoniae, Pseudomonas aeruginosa, and Proteus mirabilis--isolated from patients with pneumonia or empyema inactivated the elastase-inhibitory capacity of alpha 1-PI in vitro. These results show that in empyemas functional levels of alpha 1-PI were too low to inactivate granulocyte elastase and that some bacterial species may contribute to the low inhibitor potential of infected pleural fluid by direct alpha 1-PI inactivation.

Blood Proteins↗
PubMed1983

Mediation of skin temperature biofeedback effects in children.

Three studies are reported that, in general, fail to replicate an earlier investigation by this laboratory ( Suter & Loughry - Machado , 1981) in which impressive self-regulation of skin temperature by children was obtained. Mediation of skin temperature biofeedback effects is discussed. It is concluded that biofeedback self-regulation cannot be understood independently of the interpersonal, attitudinal, and cognitive context in which it occurs.

Adult↗
PubMed1983

High levels of complement breakdown products in tuberculous pleural effusions.

Pleural fluids from 10 patients with tuberculous pleural effusions contained high levels of small molecular weight breakdown products of C3 (C3d) and of properdin factor B (Ba) when compared to 16 patients with effusions of neoplastic origin (P less than 0.001). The same fluids exhibited overlapping values of haemolytic factor B, classical or alternative pathway-mediated haemolytic activity and native C3. A significant correlation between Ba and lysozyme levels was found in all effusions tested (P less than 0.05). These findings suggest that activation of the complement system is an important aspect of the extensive inflammation and tissue destruction characteristic of human tuberculosis.

Complement Activation↗
PubMed1983

In vitro efficacy of several antibiotics against intracellular S. aureus in chronic granulomatous disease.

We report the case of a one-year-old boy with chronic granulomatous disease (CGD), characterized by a defect in the polymorphonuclear leukocytes (PMN) which ingest, but do not kill catalase-positive bacteria such as S. aureus. This well-known observation led us to study the ability of clindamycin, rifampin, co-trimoxazole (TMP-SMX), methicillin and gentamicin to kill intracellular S. aureus in CGD and in normal PMN. Clindamycin killed S. aureus more effectively when these bacteria were intracellular than in the absence of PMN; rifampin was equally active on the same microorganisms in presence and absence of PMN, whereas TMP-SMX, methicillin and gentamicin were less effective in killing intracellular S. aureus. Similar results were obtained in CGD and in normal PMN. These results suggest that clindamycin and rifampin would be a reasonable choice in the treatment of staphylococcal infections in patients with CGD.

Anti-Bacterial Agents↗
PubMed1982

Deficient phagocytosis secondary to breakdown of opsonic factors in infected exudates.

Pleural empyema, a clinical entity characterized by the simultaneous presence of large number of PMNLs and viable bacteria, is a biological paradox which has not been fully explained yet. Our preliminary studies suggest that receptor and bactericidal functions of PMNL isolated from purulent exudates, can be close to normal in this condition. Supernatants of these empyemas however have been shown to be low in heat labile opsonic activity and complement hemolytic activity. These observations have been extended by the demonstration of breakdown of IgG, C3 and factor B in infected pleural effusions as opposed to pleural fluids obtained under other conditions. The breakdown of Ig and C3 seems to be enzymatic and to occur, at least for C3, even in the absence of Ca and Mg ions: thus, direct cleavage of C3, possibly by PMNL enzymes, has to be postulated to explain these results. Present work in our laboratory is trying to explore this possibility.

Abscess↗